2-cardio Flashcards
what is the role of the sinoatrial node
its the fastest pacemaker and dominates the rhythm normally
what is the fastest pacemaker of the heart
SA node(cells have the quickest rate of spontaneous depolarization, thus they initiate action potentials the quickest)
what is the role of the atrioventricular node node (3)
secondary pacemaker, takes over if SA node is damaged
protects ventricles from excessive electrical activity in supraventricular tissues
what part of the heart protects from excessive electrical activity in supraventricular tissues
the AV node
what is the role of the purkinje fibres
some pacemaker activity, can help if both SA AV node fail
what are the 3 phases of normal cardiac activity (simple)
atrial systole, delay, ventricular systole
where does the impulse originate that causes contraction of all the ventricles
SA node
what are the 6 steps of cardiac activity starting from SA node to ventricular contraction
1-impulse from SA node 2-atrial contraction 3-AV node 4-bundle of His 5-Purkinje fibres 6-ventricles contract
what does “extinguish by collision” mean and why do you need it
impulses from SA node divide and pass through the heart, causes collisions with all the impulses so they stop
what happens if the SA node impulse is not extinguished
then there may be extra beats or dysrhythmias
what can cause dysrhytmias (general)
when the timing of impulse passing or conduction is disturbed
what is the definition of dysrythmia
changes in normal cardiac rhythm
what can cause dysrhythmias (4 causes)
delayed after depolarization
abnormal pacemaker activities
heart block
re-entry
what is heart block/what causes it
SA fails so purkinje and AV can make contractions but they are out of pace
what are symptoms of dysrhythmias
palpatations, fainting or asymptomatic
can dysrhythmias be fatal
yes
how do you name dysrhythmias
named after point of origin
ex: atrial dysrhythmias
ventricular dysrhythmias
what is the order of flutter tachycardia and fibrillation from most to least impulses per min
fibrillation>flutter>tachycardia
what do supra ventricular dysrhythmias do to the heart (where affected)
ventricular contraction is effected but the issue is from places above (supra) the ventricles
are ventricular dysrhythmias or supraventricular dysrhythmias more dangerous than supraventricular
ventricular dysrhythmias
when do you use AV blocking drugs
for superventricular dysrhythmias
can you use AV blockers for superventricular dysrhythmias
yes its ideal
can you use AV blockers for ventricular dysrhythmias
no
you want to get it back to normal sinus rhythm
where are the “fast” cardiac action potentials
purkinje fibres, atria, ventricles
where are the “slow” cardiac action potentials
SA and AV nodes
what happens in phase 0 of purkinje AP
Na goes in (rapid depolarization)
what happens in phase 1 of purkinje AP
Na goes in to a lesser extent, L type ca channels open
what happens in phase 2 of purkinje AP
-Na Ca go through ion channels
-electrogenic na/ca exchange operates (3na in 1 ca out)
“plateau”
what happens in phase 3 of purkinje AP
K goes out (final repolarization)
what happens in phase 4 of purkinje AP
pacemaker depolarization
- Na K dependent
- activation of HCN channels
- NaK pump restores ionic gradient
what happens in phase 0 of SA node AP
Ca++ and Na+ go in
what happens in phase 1 of SA node AP
doesnt exist
what happens in phase 3 of SA node AP
K+ goes out
what happens in phase 2 of SA node AP
doesnt exist
what happens in phase 4 of SA node AP
Ca++ dependent pacemaker
does purkinje or SA node have a more Ca++ dependent action potential
SA node more Ca++
what is APD
action potential duration
what is ERP
effective refractory period
can tissue respond to stimulus during refractory perioud
no
what is the relationship between ADP and ERP
if ADP increases then ERP increases too
other way around too
what is the P wave
atrial depolarization
what is the QRS complex
ventricular depolarization
what is the T wave
ventricular repolarization
what is the PR interval
AV conduction time
what is the QT interval
duration of ventricular AP
what are 2 directions that impulses can travel
in normal or retrograde direction (so like forwards and backwards)
what happens to impulse direction with damaged tissue
normal conduction blocked BUT retrograde impulses propagate slowly
what is worse - no conduction in heart or a blocked normal conduction and slow retrograde
when its block normal and slow retrograde
what happens with a one way conduction block (what does it cause)
dysrhythmia
which adrenergic receptors are found in the heart
beta1
where are b1 receptors in the heart
all parts!
how are b1 effects of the heart mediated
by Gs (adenylyl cyclase, cAMP, phosphorylation of ion channels via PKA)
what causes the positive chronotropic effect (general)
the effect of b1 adrenergics on the heart
what happens specifically in the positive chronotropic effect (2)
increase of slope of phase 4 pacemaker in SA node
resting membrane potential gets to threshold sooner
what causes the positive ionotropic effect
increase ca influx through L type ca channels in phase 2 = more contraction (more calcium=more contraction)
what happens to AV conduction with b1 agonist and what does it cause
decreases PR interval (increase AV conduction)
enables high HR but can lead to dysrhythmia
what do b1 agonists do to ventricular AP duration
enables high HR but can lead to dysrhythmia (can make AP shorter to get more impulses in but overstimulation can cause dysrhythmia)
what do b1 agonists do to purkinje fibre (2)
increase its rhythmicity (increases slope so it gets to threshold sooner)
good for emergency pacemaker but can lead to dysrhythmias
when do early afterdepolarizations occur
in the platea
when do late afterdepolarizations occur
from resting potential
what causes late and early afterdepolarizations to occur
calcium overload, so then excess activation of Na/Ca exchanger!!1
what can happen with late and early afterdepolarizations
dysrhythmias
what is transporter in the Na Ca exchanger and where
3na in
1ca out
what nerve is the main parasympathetic nerves in the heart
vagus nerve
where does the vagus nerve go in the heart
only goes to supraventricular tissue
where do sympathetic nerves go to the heart
everywhere
what types of receptors mediate parasympathetic effects on heart
M2 receptors (muscarinic)
what g protein is M2
Gi
what causes the negative chronotropic effect (general)
M2 agonists onto the heart
what 3 main things happen in the negative chrontropic effect
SA node slows
M2 hyperpolarizes SA node (activates GIRK)
decrease slope of pahse 4 pacemaker
what are 6 main effects of b1 agonists on heart
- positive chonotropic effect
- positive inotropic effect
- AV conduction increase
- shorten ventricular AP duration
- increase purkinje fiber rhythmicity
- facilitation of generations of early/late afterdepolarization
what are 3 main effects of M2 on heart
- negative chronotropic effect
- atria shortens AP & refractory
- AV node increases PR interval
what does M2 do to atria
shortens AP duration and reduces refractory period
what does M2 do to AV node
conduction block or delay, increased PR interval
why does AV conduction increase with beta adrenergics
because they increase SA node so the ventricles gotta keep up
what does atropine do to heart
tachycardia and increased AV conduction
